Comparison of electromagnetic neuronavigation system and free-hand method for ventricular catheter placement in internal shunt

International audienc

Facteurs de risque de shunt dépendance chez les patients présentant une hémorragie intraventriculaire neonatale

National audienc

Post hemorrhagic hydrocephalus and neurodevelopmental outcomes in a context of neonatal intraventricular hemorrhage: an institutional experience in 122 preterm children

Abstract Background Intraventricular hemorrhage (IVH) is a frequent complication in extreme and very preterm births. Despite a high risk of death and impaired neurodevelopment, the precise prognosis of infants with IVH remains unclear. The objective of this study was to evaluate the rate and predictive factors of evolution to post hemorrhagic hydrocephalus (PHH) requiring a shunt, in newborns with IVH and to report their neurodevelopmental outcomes at 2 years of age. Methods Among all preterm newborns admitted to the department of neonatalogy at Rouen University Hospital, France between January 2000 and December 2013, 122 had an IVH and were included in the study. Newborns with grade 1 IVH according to the Papile classification were excluded. Results At 2-year, 18% (n = 22) of our IVH cohort required permanent cerebro spinal fluid (CSF) derivation. High IVH grade, low gestational age at birth and increased head circumference were risk factors for PHH. The rate of death of IVH was 36.9% (n = 45). The rate of cerebral palsy was 55.9% (n = 43) in the 77 surviving patients (49.4%). Risk factors for impaired neurodevelopment were high grade IVH and increased head circumference. Conclusion High IVH grade was strongly correlated with death and neurodevelopmental outcome. The impact of an increased head circumference highlights the need for early management. CSF biomarkers and new medical treatments such as antenatal magnesium sulfate have emerged and could predict and improve the prognosis of these newborns with PHH

Validation of the superior interhemispheric approach for tuberculum sellae meningioma

International audienceObjectThe objective of this study was to evaluate the ophthalmological outcome, nonvisual morbidity, and surgical complications after tuberculum sellae meningioma (TSM) removal using a superior interhemispheric approach.MethodsIn the last decade, 20 consecutive patients with TSM underwent operations using the superior interhemispheric approach. Visual acuity, visual field, and ocular fundus examination were assessed both preoperatively and 6-months postoperatively. Nonvisual morbidity was determined at an early postoperative period and at 6 months based on assessment of the Karnofsky Performance Scale score, leakage of CSF, endocrinological status, and olfactory function, which was assessed using a visual analog scale (VAS). The potential brain injury related to the approach was assessed by MRI at 6 months. Magnetic resonance imaging was then performed yearly to detect a recurrence. The mean follow up was 56.3 ± 34 months.ResultsThe primary presenting symptom for diagnosis of TSM in 20 patients (female:male ratio of 6.6:1, mean age 59.1 ± 11.1 years) was visual disturbance in 12 patients (60%), headache in 4 (20%), cognitive alteration in 1 (5%), epilepsy in 2 (10%), and accidental in 1 (5%). In a total of 40 eyes, 17 eyes in 11 patients presented with preoperative deterioration of visual acuity. Postoperatively, the visual acuity improved in 13 eyes in 8 patients (72.8%), remained unchanged in 3 eyes in 2 patients (18.2%) and deteriorated in 1 patient (9%). The nonvisual morbidity included olfactory deterioration in 7 patients (35%), and panhypopituitarism in 1 patient (5%). No patients experienced a CSF leak. The impact of olfactory deterioration on the quality of life, as estimated by a VAS score (range 0–10), was a mean of 5.7 ± 2.2 (95% CI 4.1–7.3). On the follow-up MRI, no additional lesions or recurrences were observed on the medial aspect of the frontal lobe along the surgical corridor.ConclusionsThe superior interhemispheric approach appears to be effective in resolving the problem of visual deterioration due to a TSM, without inducing surgical injury on the brain surface along the surgical corridor. Olfactory deterioration remained the challenging predominant nonvisual morbidity using this approach

Characterization of a mouse model of subarachnoid haemorrhage. Involvement of the urotensin II peptide system on vasospasm and neurosensitivomotor deficits

invited lectureInternational audienc

Characterization of a mouse model of subarachnoid haemorrhage. Involvement of the urotensin II peptide system on vasospasm and neurosensitivomotor deficits

invited lectureInternational audienc

Association between vasoactive peptide urotensin II in plasma and cerebral vasospasm after aneurysmal subarachnoid hemorrhage: a potential therapeutic target

International audienceObjective : Cerebral vasospasm (VS) is a severe complication of aneurysmal subarachnoid hemorrhage (SAH). Urotensin II (UII) is a potent vasoactive peptide activating the urotensin (UT) receptor, potentially involved in brain vascular pathologies. The authors hypothesized that UII/UT system antagonism with the UT receptor antagonist/biased ligand urantide may be associated with post-SAH VS. The objectives of this study were 2-fold: 1) to leverage an experimental mouse model of SAH with VS in order to study the effect of urotensinergic system antagonism on neurological outcome, and 2) to investigate the association between plasma UII level and symptomatic VS after SAH in human patients.METHODSA mouse model of SAH was used to study the impacts of UII and the UT receptor antagonist/biased ligand urantide on VS and neurological outcome. Then a clinical study was conducted in the setting of a neurosurgical intensive care unit. Plasma UII levels were measured in SAH patients daily for 9 days, starting on the 1st day of hospitalization, and were compared with plasma UII levels in healthy volunteers.RESULTSIn the mouse model, urantide prevented VS as well as SAH-related fine motor coordination impairment. Seventeen patients with SAH and external ventricular drainage were included in the clinical study. The median plasma UII level was 43 pg/ml (IQR 14-80 pg/ml). There was no significant variation in the daily median plasma UII level (median value for the 17 patients) from day 0 to day 8. The median level of plasma UII during the 9 first days post-SAH was higher in patients with symptomatic VS than in patients without VS (77 pg/ml [IQR 33.5-111.5 pg/ml] vs 37 pg/ml [IQR 21-46 pg/ml], p < 0.05). Concerning daily measures of plasma UII levels in VS, non-VS patients, and healthy volunteers, we found a significant difference between SAH patients with VS (median 66 pg/ml [IQR 30-110 pg/ml]) and SAH patients without VS (27 pg/ml [IQR 15-46 pg/ml], p < 0.001) but no significant difference between VS patients and healthy volunteers (44 pg/ml [IQR 27-51 pg/ml]) or between non-VS patients and healthy volunteers.CONCLUSIONSThe results of this study suggest that UT receptor antagonism with urantide prevents VS and improves neurological outcome after SAH in mice and that an increase in plasma UII is associated with cerebral VS subsequent to SAH in humans. The causality link between circulating UII and VS after SAH remains to be established, but according to our data the UT receptor is a potential therapeutic target in SAH

Vasoactive peptide urotensin II in plasma is associated with cerebral vasospasm after aneurysmal subarachnoid hemorrhage and constitutes a potential therapeutic target

National audienceOBJECTIVECerebral vasospasm (VS) is a severe complication of aneurysmal subarachnoid hemorrhage (SAH). Urotensin II (UII) is a potent vasoactive peptide activating the urotensin (UT) receptor, potentially involved in brain vascular pathologies. The authors hypothesized that UII/UT system antagonism with the UT receptor antagonist/biased ligand urantide may be associated with post-SAH VS. The objectives of this study were 2-fold: 1) to leverage an experimental mouse model of SAH with VS in order to study the effect of urotensinergic system antagonism on neurological outcome, and 2) to investigate the association between plasma UII level and symptomatic VS after SAH in human patients.METHODSA mouse model of SAH was used to study the impacts of UII and the UT receptor antagonist/biased ligand urantide on VS and neurological outcome. Then a clinical study was conducted in the setting of a neurosurgical intensive care unit. Plasma UII levels were measured in SAH patients daily for 9 days, starting on the 1st day of hospitalization, and were compared with plasma UII levels in healthy volunteers.RESULTSIn the mouse model, urantide prevented VS as well as SAH-related fine motor coordination impairment. Seventeen patients with SAH and external ventricular drainage were included in the clinical study. The median plasma UII level was 43 pg/ml (IQR 14-80 pg/ml). There was no significant variation in the daily median plasma UII level (median value for the 17 patients) from day 0 to day 8. The median level of plasma UII during the 9 first days post-SAH was higher in patients with symptomatic VS than in patients without VS (77 pg/ml [IQR 33.5-111.5 pg/ml] vs 37 pg/ml [IQR 21-46 pg/ml], p < 0.05). Concerning daily measures of plasma UII levels in VS, non-VS patients, and healthy volunteers, we found a significant difference between SAH patients with VS (median 66 pg/ml [IQR 30-110 pg/ml]) and SAH patients without VS (27 pg/ml [IQR 15-46 pg/ml], p < 0.001) but no significant difference between VS patients and healthy volunteers (44 pg/ml [IQR 27-51 pg/ml]) or between non-VS patients and healthy volunteers.CONCLUSIONSThe results of this study suggest that UT receptor antagonism with urantide prevents VS and improves neurological outcome after SAH in mice and that an increase in plasma UII is associated with cerebral VS subsequent to SAH in humans. The causality link between circulating UII and VS after SAH remains to be established, but according to our data the UT receptor is a potential therapeutic target in SAH